The world’s authority on environmental causes of cancer argues that breast cancer can largely be prevented by minimising a variety of dietary, environmental and lifestyle risks.
Breast cancer is frightening
because it appears to be so random and unavoidable. At the same time that we hear how many more women are being diagnosed with breast cancer every year now more than 186,000 in the US and 33,000 in the UK news reports and magazine articles tell us how little science knows about what causes cancer and how to prevent it. Not a day goes by, it seems, without the announcement of a new avenue of genetic research or developments in diagnostic or treatment strategies. But only a very small percentage of all breast cancer cases have a direct genetic cause.
The most important story the story that could truly save lives is not being told. Contrary to popular belief, you do have significant control over your risks of breast and other types of cancers.
Cancer does not strike randomly, but requires certain conditions, exposure to toxic substances, or both, to occur. Just as most cases of heart disease are triggered by a combination of high fat foods and a lack of physical activity, most cases of breast cancer can be traced to one or a combination of risks (see box below).
The role of oestrogen
The evidence is overwhelming that oestrogen is intimately connected to the development of most breast cancer. Under oestrogen’s influence, cells multiply and swell in preparation for possible milk production. Oestrogen encourages breast cells to divide more often and more rapidly. Thus if a mutation (inherited or triggered by a carcinogen) lies embedded in the DNA, cancer cells are more likely to proliferate when oestrogen levels are high.
We now know that two distinct types of breast cancer exist: the far more common oestrogen dependent breast cancer, influenced primarily by oestrogen, and the less common non oestrogen dependent breast cancer. More than two thirds of women with breast cancer have oestrogen dependent cancers, and that number is increasing at a particularly alarming rate. According to a 1990 study, the incidence of oestrogen dependent breast cancers, particularly among postmenopausal women, increased by 130 per cent from the mid 1970s to the mid 1980s, in contrast to only a 27 per cent increase in non oestrogen dependent cancers (J Nat Cancer Inst, 1990; 82: 693-6).
Why is oestrogen dependent breast cancer so much more common today than it was just a few decades ago? Plainly speaking, the average woman is exposed to more oestrogen over a longer period of time than ever before and at the same time, she is exposed to more carcinogenic, or “bad” oestrogen, than women were in the past.
According to one major study, the risk associated with having an early menarche for instance, one that takes place at the age of 10 is approximately twice that associated with a menarche that occurs much later, say at the age of 16 or so (Nature, 1989; 338: 389-94).
The same kind of risk profile exists at the other end of the fertility cycle: the younger a woman is at menopause, the lower her risk of breast cancer.
The good news is that you do have some control over the length of time your body naturally produces oestrogen: a recent study of some 200 women between 17 and 22 found that those whose diets were high in fibre and low in animal fat had a later menarche and subsequently fewer ovulatory and menstrual cycles than did those whose diet included more high fat, low fibre foods (Human Nutrition: Clinical Nutrition, 1986; 40C: 81-6).
Vigorous exercise on a regular basis also works to delay the onset of menarche. These factors reduce the risk of breast cancer by closing the oestrogen “window” sooner than may have otherwise occurred (see below).
Pregnancy and breastfeeding
In the context of breast cancer risk, only when a woman goes through a full term pregnancy do her breasts reach full development. Until then, the immature breast cells are more susceptible to abnormal changes stimulated by oestrogen, as well as by a wide range of cancer causing pollutants. Studies show that breast tissue is especially sensitive to exposure to environmental carcinogens that occur between a woman’s first period and her first pregnancy.
That is one reason why bearing a child helps reduce the risk of breast cancer particularly premenopausal cancer for most women. Childless women over the age of 45 run a risk from 20 to 70 per cent higher than that of women who have given birth (Epidem Reviews, 1993; 15: 36-47). Experimental studies show that mature breast cells are 50 per cent less susceptible to the risk of breast cancer induced by a chemical carcinogen than are immature cells.
Another reason pregnancy reduces the risk of breast cancer is that the period during and after gestation effectively closes the oestrogen window. Although there is an initial oestrogen surge at the very beginning of pregnancy, oestrogen levels decrease quickly and then progesterone levels soar. High levels of progesterone help to mature the breast cells and bring them to a more stable and quiescent state as they prepare for milk production. These mature cells reproduce more slowly and thus are more resistant to carcinogenic influences. Furthermore, during pregnancy and for several months after full term birth, breast fluid contains lower amounts of oestrogen than are usually present.
Because each pregnancy you carry to term further matures your breast tissue, the more children you have, the lower your risk of breast cancer. Women who have at least five full term pregnancies have half the risk of those who never bear children (Soz Praventivemed, 199; 34: 101-7). An important exception to this is for those women with a family history of breast cancer. Early, repeated pregnancies seem to increase the risk for them.
In 1995, the latest in a long litany of studies showed that women who breastfeed for 17 months or longer had a reduction in breast cancer risk of about 30 per cent (Cancer Causes and Control, 1995; 6: 199-208). When your baby suckles at your breast, that action sends a signal to the hypothalamus, which then inhibits the release of oestrogen and other hormones, thus effectively closing the oestrogen window while you breastfeed and for a number of months afterward. Studies also show that breastfeeding reduces the levels of carcinogens that concentrate in the breast and other body fat. A 1994 study of Canadian women who breastfed their babies found that the longer they had done so, the lower the levels of DDE (dichlorodiphenyldi-chloroethylene), a byproduct of the pesticide DDT, in their breast milk (J Nat Cancer Inst, 1994; 86: 803). DDE concentrations in women who’d never breastfed were about twice those of women who had breastfed 12 months or longer. Other studies show that this reduction becomes more pronounced, the more children a woman bears and breastfeeds.
Oestrogen replacement and the Pill
By taking the Pill, you expose breast tissue to higher than normal amounts of oestrogen. The Pill works by maintaining high levels of oestrogen in the body in order to prevent the ovaries from releasing eggs. The first oral contraceptives contained high doses of mestranol (ethinyloestradiol methyl ether) a relatively weak synthetic oestrogen and a synthetic progesterone or progestogen. In the late 1970s, scientists developed a “second generation” Pill, one that delivered lower doses of ethinyl oestradiol, a highly potent synthetic oestrogen. Because the doses of oestrogen and progestogen are lower in the second generation Pill than in the first, it is hailed as being safer. However, several factors indicate just the opposite.
The type of oestrogen used in the first generation Pill is half as potent as the type used in the second generation Pill. Also, unlike ethinyl oestradiol, mestranol does not bind to oestrogen receptors in the breast.
Most women who used the first generation Pill did so for a relatively short time, usually starting in their 20s. Women using the second generation Pill tend to do so for longer, sometimes starting in their teens and continuing to menopause, thus putting breast tissue under constant hormone stimulation. Most studies that have been performed on the Pill were based on the first generation form. Most women in the 1980s and 1990s use the second generation Pill.
In 1995, a National Cancer Institute study found that a few months’ use of oral contraceptives could increase the risk of breast cancer by 30 per cent; a more than twofold risk was found with 10 years of use or longer (J Nat Cancer Inst, 1995; 87: 827-35). Eleven published studies have shown an increased risk of breast cancer with the Pill; a 1990 analysis of 32 studies revealed a “statistically positive trend” in the risk of premenopausal breast cancer for women exposed to OCs for longer duration (Cancer, 1990; 2253-63). The main risk was among women who’d used the Pill for at least four years before their first full term pregnancy. And progestogen only forms of third generation pills also show a 30 per cent increased risk (New Eng J Med, 1986; 315: 405-11).
According to reviews pooling earlier studies, hormone replacement therapy is responsible for up to 8 per cent of all postmenopausal breast cancers in the United States (Am J Epidemiology; 1991; 134: 1396-1401). A series of well controlled human studies and reviews conducted over the last two decades clearly shows that extended use and high dosages of HRT increase the risk of breast cancer by about 30 to 70 per cent. This statistic means that a 70 year old woman on HRT may increase her chances of breast cancer from one in 14 to up to one in five and even higher still if she has a family history of breast cancer. In 1995, the Harvard Nurses’s Health Study confirmed these statistics, adding that prolonged use (over five years) has a particularly significant impact on health (New Eng J Med, 1995; 332: 1589-93). (For further details of specific studies, see the WDDTY Guide to the Menopause).
Dietary fat contains a wide range of contaminants pesticides, industrial pollutants and sex hormones known to cause breast cancer and/or to have oestrogenlike effects (pseudo-oestrogens). Several contaminants, including the pesticide atrazine, have both carcinogenic and oestrogenic effects, which makes them particularly dangerous. Once in your system, these contaminants tend to accumulate and concentrate in body and breast fat at levels thousands of times greater than in food, thus putting the breast at special risk.
The most dangerous of such chemicals are: pesticides; sex and growth hormones that bolster meat and dairy production; plastic wrapping and packaging; food colouring dyes; and radioactive pollutants from nuclear plants.
In 1993, researchers found that women with the highest food levels of DDE were at a four times greater risk for breast cancer, compared to those with the lowest levels (J Nat Cancer Inst, 1993; 85: 648-52). In 1994, Canadian researchers reported that concentrations of a wide range of carcinogenic and pseudo oestrogenic pesticides and pollutants were higher in the fat and blood of women with oestrogen sensitive breast cancers than in healthy women (J Nat Cancer Inst, 1994; 86: 232-4).
Dark and deadly
Another major lifestyle hazard is hair dye. Permanent and semipermanent hair dyes are a witches’ brew of carcinogens and contaminants, including diaminotoluene, diaminoanisole and other phenylenediamine dyes; dioxane, found in detergents and solvents; nitrosamines; and formaldehyde releasing preservatives. Both animal and human studies show that the body rapidly absorbs chemicals in permanent and semipermanent dyes through the skin during the more than 30 minutes the dyes remain on the scalp.
Five studies in the late 1970s found links between use of dyes and breast cancer. A 1976 study reported that 87 of 100 breast cancer patients had been long term hair dye users (NY State J of Med, 1976; 76: 394-6).
A 1979 US study found a significant relationship between frequency and duration of hair dye use and breast cancer (J Nat Cancer Inst, 1979; 62: 277-83). Those at greatest risk are 50 to 79 year olds, suggesting that the cancer takes years to develop. Women who start at age 20 have over twice the risk of 40 year olds.
Another conclusion is that the darker the shades of permanent and semipermanent dyes, the higher the risks of breast cancer.
Finally, one study found that women who dye their hair to change its colour, rather than masking greyness, were at a three fold risk (J Nat Cancer Inst, 1980; 64: 23-8).
Recently, a jointly funded American Cancer Society and Food and Drug Administration study admitted a fourfold increase in relatively uncommon cancers, including non Hodgkin’s lymphoma (the cancer that killed dark haired Jacqueline Onassis) and multiple myeloma in hair dye users (J Nat Cancer Inst, 1994; 86: 215-310).
!ADr Samuel Epstein and David Steinman
Dr Samuel Epstein, author of The Politics of Cancer, is a world authority on environmental causes of cancer. His and David Steinman’s book, The Breast Cancer Prevention Program, is available in paperback from Macmillan, 1633 Broadway, New York, NY 10019-6785 US. $14.95).